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Old 07-18-2008, 02:26 PM   #2
JokeyLoki
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AUTHOR AND EDITOR INFORMATION
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Author: J David Lane, MD, Chief, Section of Vascular and Interventional Radiology, Assistant Professor, Radiology and Nuclear Medicine, Walter Reed Army Medical Center

J David Lane is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, American Heart Association, American Medical Association, American Roentgen Ray Society, and Radiological Society of North America

Coauthor(s): Nick Lomis, MD, QI Coordinator, Diagnostic Radiology Service, Assistant Chief, Interventional Radiology, Diagnostic Radiology, Interventional Radiology Section, Walter Reed Army Medical Center

Editors: Zahir Amin, MD, MBBS, MRCP, FRCR, Consulting Staff, Department of Imaging, University College Hospital, UK; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Spencer B Gay, MD, Professor of Radiology, Director of Body Computed Tomography, Department of Radiology, University of Virginia Health Sciences Center; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; John Karani, MBBS, FRCR, Consulting Staff, Department of Radiology, King's College Hospital, London

Author and Editor Disclosure

Synonyms and related keywords: necrotizing cholecystitis, AAC
INTRODUCTION
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Background

Acute acalculous cholecystitis (AAC) represents inflammation of the gallbladder in the absence of demonstrated calculi. The disease process is distinct from the calculous variety, in which the primary initiating event is believed to be obstruction of the cystic duct. Acalculous cholecystitis typically occurs as a secondary event in patients who are hospitalized and acutely ill from another cause.

The diagnosis often is difficult and delayed because of comorbidities that decrease sensitivity and specificity of both clinical and imaging evaluation. A high degree of suspicion is required on the part of the physician. A much higher rate of complications is observed in acalculous cholecystitis (eg, gangrene, perforation) because of the more fulminant course and coexistent disease. As a result, some authors propose the term necrotizing cholecystitis to reflect the fact that acalculous cholecystitis does not simply represent cholecystitis without stones.
Pathophysiology

The pathophysiology of acalculous cholecystitis is multifactorial and defined incompletely. At least 3 mechanisms appear to work in concert to produce the disease, including (1) systemic mediators of inflammation and trauma, (2) biliary stasis, and (3) generalized or localized ischemia. In turn, the mechanisms often result in functional or secondary mechanical obstruction of the cystic duct from inflammation and bile viscosity.

In some settings, extrinsic compression also may contribute to the development of stasis. When it occurs, infection usually represents a secondary event and involves gram-negative enteric flora. In some patients, infection may be the primary event, as has been described with infection by Salmonella (ie, typhoid fever), Staphylococcus, and Brucella species and in AIDS-related cholecystitis with infection by cytomegalovirus and Cryptosporidium organisms.

Animal models have demonstrated the development of acalculous cholecystitis after administration of systemic mediators of inflammation. Small vessel necrosis in the gallbladder serosa and muscularis has been demonstrated after activation of factor XII–dependent pathways, platelet activating factor, endotoxin, or interleukin 2. This frequently is associated with gallbladder atony, which in turn predisposes patients to biliary stasis.

Biliary stasis results in more viscous bile, increased concentration of the detergent bile salts, and sludge formation, which increases the bile histotoxicity to the gallbladder mucosa. Fasting, parenteral nutrition, narcotic analgesics, and the postoperative state all predispose patients to biliary stasis and are found commonly in the population at risk.

Generalized or localized ischemia further predisposes patients to biliary stasis and may result in gallbladder wall necrosis and perforation. Hypovolemic, cardiogenic, or septic shock predisposes patients to ischemia as a contributing factor. At times, ischemia can be the primary cause and can occur in the setting of small vessel vasculitis or following therapeutic particulate embolization.

Individuals presenting with acalculous cholecystitis in the outpatient setting typically are older patients with microvascular disease and other comorbidities.
Frequency
United States

In cholecystitis, 7-22% of cases occur in the absence of demonstrated calculi. The variability is mostly a result of different patient populations, with a higher incidence in burn and trauma centers and in pediatric populations. As many as 90% of postoperative acute cholecystitis cases are acalculous in origin. While in the critical care setting cholecystitis frequently is acalculous, the overall incidence in this setting is estimated to be only 0.2%. On this background, a high index of suspicion is required.
Mortality/Morbidity

Complications of cholecystitis are much higher in the acalculous variety of the disease because of the variable pathophysiology, comorbid conditions, and the frequent delay in diagnosis and treatment. Perforation or gangrene occurs in 40-60% of patients. Gangrene can be either diffuse or focal and frequently is associated with perforation. Approximately 40% of cholecystitis cases complicated by perforation are acalculous. More than one half of cases of emph****atous cholecystitis are associated with acalculous disease, and these often are associated with gangrene.

The mortality rate varies widely in the literature from 9-66% and is attributed to the delayed diagnosis, more frequent complications, and concurrent disease processes.
Race

No identified racial predilection exists for acalculous cholecystitis.
Sex

Male-to-female ratio is 2-3:1 in most reported series.
Age

Average age is older than 50 years.
Clinical Details

AAC most commonly occurs in hospitalized patients without prior gallbladder disease and severe concomitant medical and surgical conditions. Known populations at risk ******* patients who are postoperative (especially after abdominal surgery), patients with extensive burns, patients with trauma, and patients receiving prolonged parenteral nutrition. Other reported associations ******* prolonged fasting, use of high-dose opioid analgesics, and mechanical ventilation.

A minority subset of patients present in the outpatient setting with symptoms that are easier to localize. Clinical and imaging evaluation are much more accurate in this setting. These patients are diagnosed earlier in their disease course and have a better prognosis.

In the pediatric population, acute cholecystitis is rare, but approximately one half of cases occur in the absence of demonstrated calculi. These patients are more likely to present in the outpatient setting and most often are treated by cholecystectomy.

The most frequent physical and laboratory findings ******* fever, right upper quadrant (RUQ) pain, nausea, leukocytosis, and elevation of liver-associated enzymes and bilirubin. All of these clinical parameters are nonspecific. In almost all instances in which it can be evaluated, abdominal pain is present; however, it is often not localized to the RUQ. Fever is present in two thirds of patients, and leukocytosis and liver function abnormalities are present in approximately 80%.
Preferred Examination

Early imaging evaluation is required, and frequently, multiple diagnostic tests are performed. No single imaging study is ideal. The 3 primary imaging modalities often are complementary, with ultrasound (US) or CT providing anatomic information and evaluation of adjacent structures and cholescintigraphy providing functional information.

US and cholescintigraphy should be the initial imaging tests performed to evaluate possible AAC.

CT is preferred if other differential possibilities are more likely or if CT needs to be performed for another indication.
Limitations of Techniques

All available modalities have a significant false-positive and false-negative rate and generally are better at excluding, rather than confirming, disease.

While it is unusual for acalculous cholecystitis to occur in the presence of a normal gallbladder, on both US and cholescintigraphy examinations, this finding can occur early in the course of the disease. In the patient with continued clinical deterioration who is either unable to be evaluated clinically or in whom clinical evaluation fails to demonstrate an alternative source, many authors recommend maintaining a low threshold for instituting empiric minimally invasive therapy in the form of percutaneous cholecystostomy.

DIFFERENTIALS
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Cholangitis, Recurrent Pyogenic
Cholecystitis, Acute
Cholelithiasis
Pancreatitis, Acute

Other Problems to be Considered

Differential diagnosis is broad because comorbid conditions typically are present, the ability to evaluate the patient's symptoms is reduced, and the nature of the most common clinical and laboratory manifestations is nonspecific. Almost any infectious or inflammatory process may result in nonspecific findings. In patients with more localized symptoms, the primary differentials ******* calculous cholecystitis, ascending cholangitis, acute hepatitis, and pancreatitis.

RADIOGRAPH
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* Intervention
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Findings

Plain film is of limited use in the diagnosis of AAC. Emph****atous cholecystitis may occur as a complication of acute cholecystitis, with more than one half of cases occurring in the setting of acalculous disease. This form of complicated cholecystitis typically is seen in older male patients with diabetes. On upright abdominal radiographs, this may present as an air-fluid level in the RUQ representing gas in the gallbladder lumen or a curvilinear gas collection conforming to the gallbladder wall in the case of intramural gas. Gas is visualized only in more severe cases on plain film. US and CT are much more radiographs, gas has a high association with gangrene and perforation.

CT SCAN
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Findings

CT often is performed as the diagnostic examination of choice in patients presenting with abdominal pain in the critical care setting or in patients with fever or leukocytosis of undefined etiology. CT offers the advantage of evaluating the entire chest and abdomen, but has the disadvantage of requiring transport to the scanner. Be familiar with the CT signs that suggest acalculous cholecystitis in the appropriate clinical setting.

On CT, the diagnosis of AAC requires 2 major criteria or 1 major plus 2 minor criteria as follows:

* Major criteria
o Gallbladder wall thickening greater than 3 mm
o Subserosal halo, ie, gallbladder wall edema
o Pericholecystic fatty inflammation
o Pericholecystic fluid (without ascites or hypoalbuminemia)
o Mucosal sloughing
o Intramural gas
* Minor criteria
o Gallbladder distention (>5 cm transverse)
o High-attenuation bile (sludge)

The normal gallbladder wall is barely perceptible as a thin enhancing rim on contrast-enhanced CT. In the absence of gallstones, imaging relies on ancillary findings of cholecystitis.

CT findings described in AAC are as follows:

* Gallbladder wall thickening
* Mucosal irregularity
* Luminal distention
* Increased bile density (biliary sludge)
* Intramural or intraluminal gas
* Intraluminal hemorrhage
* Localized pericholecystic fluid collections
* Inflammatory infiltration of pericholecystic fat
* Indistinctness of the liver-gallbladder interface

Degree of Confidence

While mucosal sloughing and intramural gas are specific findings, they are observed infrequently. Isolated local pericholecystic fluid collections and pericholecystic inflammatory changes are relatively specific and suggest advanced disease, but they lose specificity in the setting of ascites, recent abdominal surgery, or anasarca.

Reported sensitivity and specificity vary but generally have been greater than 90-95%. As with other imaging modalities, specificity of many of these findings is decreased in the typical populations at risk for acalculous cholecystitis because of comorbid conditions, such as recent surgery or trauma, multisystemic organ failure, ascites, or hypoalbuminemia.

ULTRASOUND
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Findings

Usually, sonography is the first examination performed in cases of possible acalculous cholecystitis. US has the advantage of being readily available, portable to the bedside, and able to identify other adjacent pathology. Primary disadvantages of US ******* the high incidence of nonspecific abnormal examinations and the inability to survey the entire abdomen.

The normal gallbladder has sonolucent bile, a thin wall, and no localized pain. Sonographic signs compatible with acalculous cholecystitis ******* the following:

* Gallbladder wall thickening
* Sonographically localized tenderness over the gallbladder
* Subserosal edema
* Pericholecystic fluid
* Gallbladder distension
* Biliary sludge
* Presence of gas

Failure of the gallbladder to contract after cholecystokinin infusion has been reported as an additional criterion, but the response often is too variable to be of use in this population.

On US, the diagnosis of AAC requires 2 major criteria or 1 major plus 2 minor criteria as follows:

* Major criteria
o Gallbladder wall thickening greater than 3 mm
o Striated gallbladder, ie, gallbladder wall edema
o Sonographic Murphy sign (ie, localized gallbladder tenderness)
o Pericholecystic fluid (without ascites or hypoalbuminemia)
o Mucosal sloughing
o Intramural gas
* Minor criteria
o Gallbladder distention (>5 cm transverse)
o Echogenic bile (sludge)

Gallbladder wall thickness should be measured in the transverse plane in a noncollapsed gall bladder. The presence of ascites or decreased oncotic pressure (as with hypoalbuminemia) confuses the finding, unless the finding is markedly discordant. Similarly, pericholecystic fluid is not meaningful in the presence of generalized ascites, but when occurring as a localized finding, it often signifies advanced disease or perforation. Sonographic Murphy sign is the most specific sonographic finding, but often it cannot be evaluated because of the patient's clinical condition.

Diagnostic needle aspiration of the gallbladder for bile Gram stain and culture often is normal with a sensitivity of less than 50%, and the results of culture are delayed. Therefore, the test is of limited value for the diagnosis of AAC. Culture is performed routinely at the time of therapeutic cholecystostomy and may guide antibiotic selection.
Degree of Confidence

Sensitivity and specificity of sonography in acalculous cholecystitis varies from 23-95% and 40-95%, respectively, because of the variable patient populations, clinical course, and imaging technology over the reported time periods. Sensitivity and specificity are greater than 90% in the subset of patients who present in the outpatient setting with acalculous cholecystitis.

Overall, sensitivity and specificity approach 70%. As the proportion of patients in the critical care environment increases, the diagnostic accuracy decreases. Several recent studies have documented the high incidence of abnormal gallbladder sonograms in the ICU environment in asymptomatic patients not suspected of having acalculous cholecystitis.

At least one abnormal finding was seen in 50-85% of patients in this setting, with 3 abnormal findings seen in as many as 57% of patients. None of these patients had localized gallbladder tenderness by sonography. Serial sonography has been of benefit in some studies with a progressively worsening appearance on short-term follow-up images improving the specificity for diagnosis.

NUCLEAR MEDICINE
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Findings

Hepatobiliary scintigraphy (HBS) is a physiologic test that evaluates hepatic bile formation, excretion, and ductal functional patency.

Imaging typically is performed with dynamic image acquisition for up to 4 hours following the intravenous (IV) administration of 5 mCi of a technetium Tc 99m-labeled iminodiacetic acid derivative. Peak liver uptake is at 5-10 minutes, with subsequent gallbladder visualization by 20 minutes and duodenal visualization by 30 minutes.

If nonvisualization or questionable visualization of the gallbladder occurs, but adequate hepatic uptake and excretion into the bowel is seen, IV morphine sulfate (0.04 mg/kg) can be administered at 30-40 minutes with imaging carried out to 1 hour. This raises intrabiliary pressure by inducing contraction of the sphincter of Oddi and filling of the gallbladder if the cystic duct remains patent. A lateral view can be helpful if a question remains of gallbladder filling with the gallbladder located anteriorly in this projection.

Others have attempted to improve accuracy by pretreating with cholecystokinin infusion prior to HBS to empty the distended gallbladder. HBS may be nondiagnostic in patients with liver failure and intrahepatic cholestasis of any cause because of the inability to conjugate and excrete the radiotracer.

Additional useful findings at cholescintigraphy ******* the presence of an area of increased pericholecystic radiotracer accumulation in the gallbladder fossa. This rim sign is associated with complications such as gangrene. Radiotracer extravasation rarely can be visualized in the setting of perforated gangrenous cholecystitis if the cystic duct remains patent.
Degree of Confidence

HBS is accurate in the diagnosis of calculous cholecystitis since the primary event is believed to be cystic duct obstruction. In acalculous cholecystitis, functional obstruction usually occurs in the disease process but is variable and is not the primary process. Not surprisingly, the sensitivity and specificity of the test are decreased in this setting.

In general, diagnostic quality studies with augmentation yield a sensitivity of 80-90% and a specificity of 90-100%.
False Positives/Negatives

The false-positive rate without pharmacologic augmentation can be as high as 40% in some series, decreasing the specificity of the test. With morphine augmentation, the false-positive rate is decreased and specificity is improved.

False-negative results (gallbladder filling in presence of acalculous cholecystitis) also can occur. Early filling of the gallbladder (within first 30 min) excludes the diagnosis of acalculous cholecystitis, but delayed filling after augmentation can be associated with a false-negative rate as high as 20%.

ANGIOGRAPHY
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Findings

No role exists for angiography in the diagnosis of acalculous cholecystitis.

INTERVENTION
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Once the diagnosis of AAC is made, the gallbladder should be removed or drained.

Therapeutic options for acalculous cholecystitis ******* open and laparoscopic cholecystectomy, surgical cholecystostomy, percutaneous cholecystostomy or aspiration, and endoscopic transcystic drainage.

Surgical cholecystectomy

Surgical cholecystectomy remains the definitive treatment. In the minority of patients presenting in the outpatient setting or with minimal comorbidity, it is the procedure of choice. Unfortunately, most patients with this diagnosis are typically found in the critical care setting or recovering from major surgery or trauma and have a high risk of operative mortality. These patients are often best managed with less invasive treatments.

Percutaneous cholecystostomy

If performed before complicated disease has occurred, such as frank necrosis or perforation, this procedure can be life-saving, definitive therapy. Initial imaging findings consistent with complicated cholecystitis or progression of signs and symptoms after PCC should still prompt cholecystectomy.

* PCC procedure
*
o PCC is an image-guided procedure performed under local anesthesia at bedside or in the interventional suite. US is used to guide placement of a drainage catheter into the gallbladder. CT is occasionally used if no suitable ultrasonographic window is found. Drainage can be accomplished using a single-step trocar drainage technique or needle access followed by serial dilation and catheter placement over a guidewire. A 6-10F locking pigtail drainage catheter with large side holes is used. While somewhat controversial, a transhepatic tract is typically favored. This has been shown to decrease the risk of catheter dislodgement and minimize the potential for bile leakage.
o After catheter placement, the gallbladder is drained and left to external drainage with daily monitoring of outputs. In the presence of viscous bile, regular flushing with 5 mL of sterile saline helps maintain catheter patency. Catheter output may be minimal until the patient improves, with decreased biliary stasis and restoration of functional cystic duct patency.
* Indications
*
o PCC is indicated when imaging and clinical findings suggest acalculous cholecystitis as the diagnosis. In some instances, imaging results are inconclusive or discordant, and clinical evaluation is nonspecific. In the absence of other treatable etiologies, proceeding with PCC on an empiric basis is reasonable to see if the patient improves. In this setting, PCC is as much a diagnostic test as a treatment. Most patients, if they are going to respond, show definitive clinical improvement within 72 hours following drainage.
* Contraindications and complications
*
o Contraindications to PCC ******* uncorrectable coagulopathy and massive ascites that cannot be drained adequately. Complications of PCC ******* bleeding, bile peritonitis, vagal reactions, catheter dislodgment, and damage to adjacent structures. The procedural complication rate is 5-10%.
o Technical success is achieved in 95-100% of patients, and clinical response is achieved in 70-85%. The 30-day mortality rate remains high at 10-30% but almost always results from underlying conditions. Many series reporting on PCC ******* patients with both calculous and acalculous disease who are not suitable candidates for surgery.
* Follow-up care
*
o Follow-up cholecystogram is performed if a question of catheter function exists, if the patient fails to respond, and if catheter removal is under consideration.
o Minimum criteria and considerations for removing PCC tubes are as follows:
o
+ Three weeks of drainage time
+ Patent cystic duct and common bile duct
+ Initial primary risk factors corrected
+ Signs and symptoms of AAC resolved
+ No or minimal ascites
* Tract maturation
*
o After 3 weeks, almost all PCC tracts are mature and will not result in significant peritoneal leakage. PCC tract maturation depends on the catheter material, catheter dwell time, the nutritional status of the patient, and the presence of steroids. If risk factors are present for delayed maturation or early tube removal is considered, a tractogram can be performed easily over a guidewire at the time of the cholecystogram.
o A tractogram (sinogram) is performed by removing the drainage catheter over a guidewire and placing a short, equivalent-size sheath into the gall bladder. While slowly withdrawing the sheath over the wire through the tract, dilute contrast in injected to evaluate the tract integrity. If extensive peritoneal leakage is identified, a new drain can be placed over the guidewire. It is best to have the initial underlying risk factors, such as parenteral nutrition and sepsis, corrected to minimize the risk of cholecystitis recurrence.

#

* Needle aspiration
*
o Therapeutic needle aspiration of the gallbladder with an 18-gauge transhepatic needle also has been reported successful in treating acute cholecystitis in high-risk surgical patients. A recent study by Chopra et al found simple aspiration to be effective in 77% of patients with AAC, whereas PCC was effective in 90% of patients.
o PCC was used as a salvage procedure in patients failing to respond clinically within 72 hours following aspiration alone, with equally good results and a lower overall complication rate. This study excluded ICU patients with acalculous cholecystitis in whom the diagnosis is more difficult and the therapeutic outcome less favorable and more difficult to assess. The findings suggest that needle aspiration is a reasonable first step in high-risk patients with AAC outside of the critical care environment.

Transpapillary endoscopic cholecystostomy

In patients in whom percutaneous drainage cannot be performed safely, transpapillary endoscopic cholecystostomy is another option. In this technique, the cystic duct is selected during endoscopic retrograde cholangiopancreatography (ERCP) and either a double pigtail biliary stent or a nasobiliary catheter is placed into the gallbladder. Technical success has been achieved in up to 90% of patients, although many of the reported series have been on less critically ill patients or those with more chronic symptoms. Advantages ******* the potential decreased risk of bleeding, bile peritonitis, and injury to adjacent organs. Disadvantages are the need for sedative medications and risks of aspiration, pancreatitis, and associated risks related to ERCP.
Medical/Legal Pitfalls

* Failure to maintain a high index of clinical suspicion, which facilitates early diagnosis and therapy and optimizes outcome.


MULTIMEDIA
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Media file 1: Abdominal radiograph of acalculous emph****atous cholecystitis demonstrating curvilinear air pattern conforming to the shape of the gallbladder wall.
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Media type: X-RAY

Media file 2: CT images of emph****atous cholecystitis (same patient as Image 1).
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Media type: CT

Media file 3: CT cine loop of acalculous cholecystitis demonstrates irregular gallbladder wall, pericholecystic inflammation, and perihepatitis in gallbladder fossa. Necrotic gallbladder was present at surgery.
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Media type: CT

Media file 4: Normal hepato-iminodiacetic acid scan. Prompt hepatic concentration of radiopharmaceutical is noted, along with early visualization of the gallbladder and drainage into the duodenum.
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Media type: Movie

Media file 5: Hepato-iminodiacetic acid scan of acalculous cholecystitis. Prompt uptake of radiopharmaceutical is noted in the liver, along with drainage into the bowel without gallbladder visualization by 90 minutes.
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Media type: Movie

Media file 6: Ultrasound of ICU patient with fever of unclear etiology. Ultrasound findings of acalculous cholecystitis ******* marked gallbladder wall thickening and pericholecystic fluid. Localized tenderness could not be evaluated.
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Media type: Image

Media file 7: Transverse ultrasound demonstrates marked gallbladder wall thickening and pericholecystic fluid collection in a patient with AIDS who was managed conservatively. No localized tenderness is noted, and hepato-iminodiacetic acid scan demonstrated delayed filling but otherwise was normal. Patient recovered with treatment of underlying pneumonia, and ultrasound findings normalized within 2 weeks.
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Media type: Image

Media file 8: A 53-year-old man status post–endoscopic stenting for pancreatic cancer with progressive fever, leukocytosis, and right upper quadrant pain. Ultrasound demonstrates gallbladder distention, biliary sludge, borderline wall thickness, and localized tenderness consistent with acalculous cholecystitis.
Click to see larger picture Click to see detailView Full Size Image
Media type: Image

Media file 9: Images from percutaneous transhepatic cholecystostomy tube placement using coaxial technique demonstrating transhepatic needle access, irregular gallbladder wall, and occluded cystic duct (same patient as Image 8). Note the safety wire adjacent to the definitive 6F drainage catheter.
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Media type: X-RAY

Media file 10: Despite drainage, the patient (same patient as Pictures 8 and 9) continued to experience right upper quadrant pain and leukocytosis. Ultrasound and CT studies demonstrate transhepatic cholecystomy catheter in good position, but interval development of markedly worsening gallbladder wall edema and pericholecystic inflammatory changes have occurred. At surgery, gangrenous gallbladder was found and resected successfully.
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Media type: CT

Media file 11: Ultrasound images from percutaneous cholecystomy using the trocar technique. Ultrasound guides transhepatic access to the gallbladder with a 6F trocar drainage catheter. After access, the catheter is fed forward to reform the distal pigtail within the gallbladder lumen and is locked in this configuration.
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Media type: Image

Media file 12: Cine image of pigtail catheter moving freely within the gallbladder, which confirms adequate placement, along with free return of bile from the catheter.
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Media type: Movie

Media file 13: Cine loop percutaneous cholecystostomy tractogram demonstrates immature tract 3 weeks after percutaneous cholecystostomy. Free spillage of contrast into the peritoneal space is noted. Drainage was continued for an additional 2 weeks prior to catheter removal.
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Media type: Movie

Media file 14: Cholecystogram 4 weeks status post–cholecystomy tube placement for acalculous cholecystitis demonstrating a patent cystic and common duct and the absence of calculi. All clinical signs and symptoms had resolved.
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Media type: X-RAY


REFERENCES
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* Boland GW, Lee MJ, Leung J, Mueller PR. Percutaneous cholecystostomy in critically ill patients: early response and final outcome in 82 patients. AJR Am J Roentgenol. Aug 1994;163(2):339-42. [Medline].
* Boland GW, Slater G, Lu DS, et al. Prevalence and significance of gallbladder abnormalities seen on sonography in intensive care unit patients. AJR Am J Roentgenol. Apr 2000;174(4):973-7. [Medline].
* Byrne MF, Suhocki P, Mitchell RM, et al. Percutaneous cholecystostomy in patients with acute cholecystitis: experience of 45 patients at a US referral center. J Am Coll Surg. Aug 2003;197(2):206-11. [Medline].
* Chopra S, Dodd GD 3rd, Mumbower AL, et al. Treatment of acute cholecystitis in non-critically ill patients at high surgical risk: comparison of clinical outcomes after gallbladder aspiration and after percutaneous cholecystostomy. AJR Am J Roentgenol. Apr 2001;176(4):1025-31. [Medline].
* Conway JD, Russo MW, Shrestha R. Endoscopic stent insertion into the gallbladder for symptomatic gallbladder disease in patients with end-stage liver disease. Gastrointest Endosc. Jan 2005;61(1):32-6. [Medline].
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Cholecystitis, Acalculous excerpt

Article Last Updated: Mar 23, 2005

 
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